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Volume 181, Issue 3, Pages 193-198 (30 March 2010)


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Differential fractional anisotropy abnormalities in adolescents with ADHD or schizophrenia

Nicholas D. DavenportaCorresponding Author Informationemail address, Canan Karatekinbc, Tonya Whitebcde, Kelvin O. Limacde

Received 4 December 2008; received in revised form 5 September 2009; accepted 23 October 2009.

Abstract 

Schizophrenia and Attention-Deficit/Hyperactivity Disorder (ADHD) are associated with similar deficits in working memory, attention, and inhibition. Both disorders also involve abnormalities of white matter integrity, possibly reflecting neural communication disruptions. There are likely some regional white matter abnormalities that underlie the common cognitive impairment, though also some regional abnormalities unique to each disorder. We used diffusion tensor imaging (DTI) to compare white matter integrity, as indicated by fractional anisotropy (FA), in adolescents with schizophrenia (n=15) or ADHD (n=14) and healthy controls (n=26). Schizophrenia patients had uniquely low FA, relative to the other two groups, in bilateral cerebral peduncles, anterior and posterior corpus callosum, right anterior corona radiata, and right superior longitudinal fasciculus. ADHD patients had uniquely high FA in left inferior and right superior frontal regions. Both clinical groups had lower FA than controls in left posterior fornix. The two disorders generally demonstrated distinct patterns of abnormal connectivity suggesting that common cognitive and behavioral deficits derive from distinct sources, though the posterior fornix may be involved in both disorders. Schizophrenia was associated with abnormally low FA in widespread circuitry indicative of general connectivity disruptions, whereas ADHD was associated with abnormally high FA in frontal networks that may indicate impaired branching of fibers.

a Department of Psychology, University of Minnesota, Minneapolis, MN, United States

b Institute of Child Development, University of Minnesota, Minneapolis, MN, United States

c Center for Neurobehavioral Development, University of Minnesota, Minneapolis, MN, United States

d Department of Psychiatry, University of Minnesota, Minneapolis, MN, United States

e Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States

Corresponding Author InformationCorresponding author. Department of Psychology, N218 Elliott Hall, 75 East River Rd., Minneapolis, MN 55455, United States. Tel.: +1 612 251 3394; fax: +1 612 626 2079.

 Presented in part at the Annual Meeting of the Society for Neuroscience, San Diego, November 2007.

PII: S0925-4927(09)00245-5

doi:10.1016/j.pscychresns.2009.10.012


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